Abstract: Pigment nephropathy defined as an abrupt decrease in renal function due to the toxic effect of endogenous haem-containing pigment on the kidney like myoglobin which released from skeletal muscle in rhabdomyolysis and free hemoglobin in intravascular hemolysis and bile pigment in cholestasis. pigment nephropathy is one of the causes of acute kidney injury labile iron playing a central role in renal sideropathy. Inflammation is the most important mechanism of pigment induced acute renal injury. Sterile inflammation is mediated through the inflammasome. The most important one is nucleotide-binding domain-like receptor protein 3 (NLRP3) which involved in most inflammatory mediated renal diseases. Inhibiting the inflammasomes may significantly reduce damaging which occurs in the kidney. Prevention playing a vital step in the management of pigment nephropathy, clinical suspicion, and biochemical investigations is a challenge to identify the risk of the condition before progression to AKI. Intravenous fluid replacement to correct hypovolemia and guard against cast formation in the renal tubules preventing progression to acute renal failure.
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